Functional neuroimaging of conversion disorder: The role of ancillary activation

Abstract

BackgroundPrevious functional neuroimaging studies investigating the neuroanatomy of conversion disorder have yielded inconsistent results that may be attributed to small sample sizes and disparate methodologies. The objective of this study was to better define the functional neuroanatomical correlates of conversion disorder.MethodsTen subjects meeting clinical criteria for unilateral sensory conversion disorder underwent fMRI during which a vibrotactile stimulus was applied to anesthetic and sensate areas. A block design was used with 4 s of stimulation followed by 26 s of rest, the pattern repeated 10 times. Event-related group averages of the BOLD response were compared between conditions.ResultsAll subjects were right-handed females, with a mean age of 41. Group analyses revealed 10 areas that had significantly greater activation (p < .05) when stimulation was applied to the anesthetic body part compared to the contralateral sensate mirror region. They included right paralimbic cortices (anterior cingulate cortex and insula), right temporoparietal junction (angular gyrus and inferior parietal lobule), bilateral dorsolateral prefrontal cortex (middle frontal gyri), right orbital frontal cortex (superior frontal gyrus), right caudate, right ventral-anterior thalamus and left angular gyrus. There was a trend for activation of the somatosensory cortex contralateral to the anesthetic region to be decreased relative to the sensate side.ConclusionsSensory conversion symptoms are associated with a pattern of abnormal cerebral activation comprising neural networks implicated in emotional processing and sensory integration. Further study of the roles and potential interplay of these networks may provide a basis for an underlying psychobiological mechanism of conversion disorder.

Cortical thickness alterations linked to somatoform and psychological dissociation in functional neurological disorders

“…Here, we specifically extend these findings by linking ACC cortical thickness to the magnitude of endorsed somatoform dissociation experienced by patients with motor FND. An extensive literature connects the ACC to the neuropathobiology of FND (Aybek, et al, 2015; Burke, et al, 2014; Mailis-Gagnon, et al, 2003; Marshall, et al, 1997; Perez, et al, 2012; Perez, et al, 2015; Saj, et al, 2009; Voon, et al, 2016), including resting state studies characterizing abnormal ACC connectivity profiles linked to dissociation (van der Kruijs, et al, 2012) and PNES frequency (Li, et al, 2015). The caudal ACC, implicated in appraisal and the behavioral expression of affective states, is structurally connected to lateral prefrontal and premotor regions (Etkin, et al, 2011).…”

Functional networks of motor inhibition in conversion disorder patients and feigning subjects

“…On the other hand, several imaging studies consistently observed activity in the IFG of CD patients with motor symptoms ( Stone et al, 2007 ), sensory ( Mailis-Gagnon et al, 2003 ), visual loss ( Werring et al, 2004 ) or amnestic disorders ( Kanaan et al, 2007 , Markowitsch et al, 1997 ). Depending on the employed experimental paradigms such as attempted movement execution ( Marshall et al, 1997 ), movement observation ( Burgmer et al, 2006 ), movement inhibition ( Cojan et al, 2009 ), mental rotation ( de Lange et al, 2010 ) or vibratory stimulation ( Burke et al, 2014 , Vuilleumier et al, 2001 ) studies have described several different neural structures to be involved or abnormally active in CD. Some of the differences could also steam from the type of paresis (flaccid or with muscle tone increase) of the CD patients that might have different neural correlates due to different levels of inhibition.…”

“…Brain areas in the lateral and medial frontal cortex as well as the supplementary motor area and basal ganglia have been suggested to be involved in this condition (for review see ( Bell et al, 2011 )). The diversity of the employed study paradigms like motor execution ( Spence et al, 2000 , Stone et al, 2007 , van Beilen et al, 2011 ), Go/Nogo ( Cojan et al, 2009 ), implicit ( de Lange et al, 2007 , de Lange et al, 2008 ) and explicit motor imagery ( Burgmer et al, 2013 , van Beilen et al, 2011 ) or vibratory stimulation ( Burke et al, 2014 , Vuilleumier et al, 2001 ) have provided a wide range of brain areas that could be involved in the clinical condition but did not isolate a core component. In addition the different and rather small sample sizes, the lack of control in motor imagery and motor execution paradigms in paretic patients as well as the heterogeneity of the included patients probably contributed to the divergent results.…”

Uncovering the etiology of conversion disorder: insights from functional neuroimaging

“…In one study, ten subjects underwent unilateral vibrotactile stimulation of their symptomatic and asymptomatic limbs. 37 Ten brain areas showed significantly greater activation when stimulation was applied to the anesthetic body part compared to the contralateral side: right paralimbic cortices (insula and anterior cingulate cortex [ACC]), the right TPJ (angular gyrus and inferior parietal lobule), bilateral DLPFC, right orbital frontal cortex, right caudate, right ventral anterior thalamus, and left angular gyrus. Mailis-Gagnon et al reported on four patients with chronic pain and non-dermatomal sensory loss, who had deactivation of somatosensory cortex along with increased activity in the right ACC during evoked potential perceived touch, or noxious stimuli compared to unperceived stimuli.…”